Dilated cardiomyopathy
Dilated cardiomyopathy: Excerpt from Professional Guide to Diseases (Eighth Edition)
Dilated cardiomyopathy results from extensively damaged myocardial muscle fibers. This disorder interferes with myocardial metabolism and grossly dilates all four chambers of the heart, giving the heart a globular appearance and shape. In this disorder, hypertrophy may be present. Dilated cardiomyopathy leads to intractable heart failure, arrhythmias, and emboli. Because this disease isn’t usually diagnosed until it’s in the advanced stages, the patient’s prognosis is generally poor.
Causes and incidence
The cause of most cardiomyopathies is unknown. Occasionally, dilated cardiomyopathy results from myocardial destruction by toxic, infectious, or metabolic agents, such as certain viruses, endocrine and electrolyte disorders, and nutritional deficiencies. Other causes include muscle disorders (myasthenia gravis, progressive muscular dystrophy, and myotonic dystrophy), infiltrative disorders (hemochromatosis and amyloidosis), and sarcoidosis.
Cardiomyopathy may also be a complication of alcoholism. In such cases, it may improve with abstinence from alcohol but recurs when the patient resumes drinking. How viruses induce cardiomyopathy is unclear, but researchers suspect a link between viral myocarditis and subsequent dilated cardiomyopathy, especially after infection with poliovirus, coxsackievirus B, influenza virus, or human immunodeficiency virus.
Metabolic cardiomyopathies are related to endocrine and electrolyte disorders and nutritional deficiencies. Thus, dilated cardiomyopathy may develop in patients with hyperthyroidism, pheochromocytoma, beriberi (thiamine deficiency), or kwashiorkor (protein deficiency). Cardiomyopathy may also result from rheumatic fever, especially among children with myocarditis.
Antepartal or postpartal cardiomyopathy may develop during the last trimester or within months after delivery. Its cause is unknown, but it occurs most frequently in multiparous women older than age 30, particularly those with malnutrition or preeclampsia. In these patients, cardiomegaly and heart failure may reverse with treatment, allowing a subsequent normal pregnancy. If cardiomegaly persists despite treatment, the prognosis is poor.
Dilated cardiomyopathy occurs in 2 of every 100 people and affects all ages and sexes. It’s most common in adult men.
Signs and symptoms
In dilated cardiomyopathy, the heart ejects blood less efficiently than normal. Consequently, a large volume of blood remains in the left ventricle after systole, causing signs of heart failure — both left-sided (shortness of breath, orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and an irritating dry cough at night) and right-sided (edema, liver engorgement, and jugular vein distention). Dilated cardiomyopathy also produces peripheral cyanosis and sinus tachycardia or atrial fibrillation at rest in some patients secondary to low cardiac output. Auscultation reveals diffuse apical impulses, pansystolic murmur (mitral and tricuspid insufficiency secondary to cardiomegaly and weak papillary muscles), and S 3 and S4 gallop rhythms.
Diagnosis
No single test confirms dilated cardiomyopathy. Diagnosis requires elimination of other possible causes of heart failure and arrhythmias.
❑ Electrocardiography (ECG) and angiography rule out ischemic heart disease; ECG may also show biventricular hypertrophy, sinus tachycardia, atrial enlargement and, in 20% of patients, atrial fibrillation and bundle-branch block.
❑ Chest X-ray shows cardiomegaly — usually affecting all heart chambers — and may demonstrate pulmonary congestion, pleural or pericardial effusion, or pulmonary venous hypertension.
❑ Chest computed tomography scan or echocardiography identifies left ventricular thrombi, global hypokinesia, and degree of left ventricular dilation.
❑ Nuclear heart scans, such as multiple-gated acquisition scanning and ventriculography, show heart enlargement, lung congestion, heart failure, and decreased movement or functioning of the heart.
Treatment
Therapeutic goals include correcting the underlying causes and improving the heart’s pumping ability with digoxin, diuretics, oxygen, and a sodium-restricted diet. Other options may involve bed rest and steroids. Vasodilators reduce preload and afterload, thereby decreasing congestion and increasing cardiac output. Acute heart failure requires vasodilation with nitroprusside or nitroglycerin I.V. Long-term treatment may include prazosin, hydralazine, isosorbide dinitrate, angiotensin-converting enzyme inhibitors, and anticoagulants.
When these treatments fail, therapy may require a heart transplant for carefully selected patients. Cardiomyoplasty, which wraps the latissimus dorsi muscle around the ventricles, assists the ventricle to effectively pump blood. A cardiomyostimulator delivers bursts of electrical impulses during systole to contract the muscle.
Special considerations
In the patient with acute failure:
❑ Monitor for signs of progressive failure (increasing crackles and dyspnea and increased jugular vein distention) and compromised renal perfusion (oliguria, elevated blood urea nitrogen and creatinine levels, and electrolyte imbalances). Weigh the patient daily.
❑ If the patient is receiving vasodilators, check blood pressure and heart rate. If he becomes hypotensive, stop the infusion and place him in a supine position, with legs elevated to increase venous return and to ensure cerebral blood flow.
❑ If the patient is receiving diuretics, monitor for signs of resolving congestion (decreased crackles and dyspnea) or too vigorous diuresis. Check serum potassium level for hypokalemia, especially if therapy includes digoxin.
❑ Therapeutic restrictions and an uncertain prognosis usually cause profound anxiety and depression, so offer support and let the patient express his feelings. Be flexible with visiting hours.
❑ Before discharge, teach the patient about his illness and its treatment. Emphasize the need to avoid alcohol, smoking, to restrict sodium intake, to watch for weight gain (a weight gain of 3 lb [1.4 kg] over 1 to 2 days indicates fluid accumulation), and to take digoxin as prescribed, and watch for its adverse effects (anorexia, nausea, vomiting, and yellow vision).
❑ Encourage family members to learn cardiopulmonary resuscitation.
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
More About Dilated cardiomyopathy
More Medical Textbooks Online about Dilated cardiomyopathy
Review other book chapters online related to Dilated cardiomyopathy:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: Hypertrophic cardiomyopathy (Professional Guide to Diseases (Eighth Edition))
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
